Summary

Knowledge of the origin and evolution of viruses could provide a better understanding of a number of
phenomena in the field of evolution such as the origin and development of multi-cellular organisms, the rapid
diversification of species over the last 600–700 million years and the lack of transitional forms in the evolution of species
(‘‘missing links’’) etc. One of the possible effects of escaped DNA/RNA sequences or viruses on the evolution of multicellular
organisms, especially vertebrates, could be the phenomenon of horizontal transmission and dissemination of
genes. Interestingly, if so, this effect could be considered as a model of primeval and natural genetic engineering. Other
possible links between the evolution of multi-cellular organisms and viruses are connected with the fact that viruses
represent the source of different forms of selective pressure such as epidemics of infectious diseases, autoimmunity,
malignant alteration, reproductive efficiency, etc. At the same time, these two models of ‘‘long-term evolutionary
relations’’ could represent ‘‘key factors’’ in the evolution between viruses and multi-cellular organisms. The capability
of a genome to produce and emit DNA/RNA sequences or de novo created viruses which can be a vector of genes
horizontal transmission and/or cause selective pressure on concurrent or predator species gives a new characteristic to
viruses – the possibility of their acting as natural biological weapons. Finally, possibly evolutionary advantages of this
genome capability could be one of explanations for the phenomena such as genome instability and its ability to emit
DNA/RNA sequences and/or de novo created viruses, as well as evolutionary conservation of this unique phenomena.

The origin and evolution of viruses

In contrast to other microbes and multi-cellular
organisms, the origin and evolution of viruses is
mostly unknown. Our knowledge concerning their
origin is lost in a sea of conjecture and speculations,
hardly supported at all with precise scientific
evidences. For example, viruses have never been
detected as fossil particles, probably because they
are too small and too fragile to succumb to fossilization
processes. Even in fossilized biological materials such as plant leaves or insects in amber,
preserved nucleic acid sequences of viruses have
never been detected. Hence, evolutionists are limited
in their ability to precisely reconstruct an evolutional
history of viruses. However, in spite of all
the difficulties in understanding their origin and
evolution, several theories more or less successfully
explain the basic observed facts [1–3].

Due to the fact that the genome of viruses
underlies mutation and genetic recombination,
viruses probably evolve according to a form of natural
selection, very similar to that governing other
living things. It seems that this simple fact may
well provide enough support for scientific acceptability
of several commonly discussed hypotheses
on virus origin and evolution. Currently, there are
three such hypotheses. The first hypothesis is the
so-called theory of ‘‘regressive evolution’’, which
proposes that viruses descend from free-living
and more complex parasites. According to this theory,
ancestral viruses developed a growing dependence
on host-cell intracellular ‘‘machinery’’
through evolutionary time, while retaining the ability
to auto-replicate, like mitochondria that have
their own genetic information and replicate on
their own [2–4]. The second hypothesis is the socalled
theory of ‘‘cell origin’’, which assumes that
viruses reflect their origin from cell DNA and/or
messenger RNA, which acquired the ability to
auto-replicate, create extracellular virions, exist
and function independently. Finally, there is the
theory of ‘‘independent’’ or ‘‘parallel’’ evolution
of viruses and other organisms, which assumes that
viruses appeared at the same time as the most
primitive organisms [1,3,4].

Whatever the advantages and disadvantages of
each theory are, the ability of every cell (excluding
cells without a nucleus, e.g., the erythrocytes of
mammals) to release DNA/RNA sequences or de
novo created viruses is unique and amazing. At
the same time, the cell’s ability to release DNA/
RNA sequences shows a high level of evolutionary
conservation. These facts might be well enough
motifs for identification of positive selective pressure
that could be linked with this genome ability,
as well as a highly important thesis for better
understanding of origin and evolution of viruses,
and even life as we know it [3–5]. Several factors
of positive selective pressure could play important
role in development and evolutionary ‘‘symbiotic’’
linking (conservation) of genome and its ‘‘instability’’,
which is probably responsible for cell ability
to emit de novo created viruses: (i) the possibility
of horizontal and vertical dissemination of gene
blocks, and their incorporation into the cell genome
of new hosts; (ii) the possibility of acceleration
of evolutionary processes, which could result
in rapid diversification of species and sometimes
quicker and better adapting to environmental conditions;
(iii) the possibility that de novo created
viruses can act as natural biological weapons
against predator and/or concurrent species.

There are a number of complex molecular life
forms that blur the boundaries between cells and
viruses. Also, there are pieces of self-replicating
genetic material found in bacteria, e.g., episomes,
which evolve independently of their hosts, and can
even move from one host to another – but carry
genetic information that may be toxic or beneficial,
even essential, to their host. In the case of
the beneficial role of episomes, many bacteria
would be unable to reproduce at all without them.
Episomes are, in many ways, quite similar to
viruses – except that they only reproduce themselves
when their hosts do, whereas viruses reproduce
themselves hundreds of times, causing
disease. According to this way of thinking, viruses
probably co-evolve with their hosts, like any ‘‘good
parasite’’. There appears to be quite a lot of justification
for this idea, especially from studies of
viruses such as papilloma viruses, endogenous retrovirus-
like sequences in animal genomes, and herpes
viruses. For example, the divergences of
primates and of birds related to chickens have been
traced by comparing the types and sequences of
retroviral-derived sequences in their genomes. It
has also been repeatedly shown that the closest
relatives of human papillomavirus types infecting
particular tissue types (e.g., cutaneous wart types,
genital mucosal types) are those viruses infecting
similar tissue types in other primates, indicating
that these tissue preferences were well established
before the divergence of humanoid apes from the
primate line [1,3,4].

Viruses as evolutionary accelerators

The model of living beings evolving based on genome
changes and the ability to adapt to positive
and/or negative selection pressures is widely accepted
among evolutionists. However, it is hard
to imagine that the evolution of life is based on
accidental and isolated gene mutations and that
this model of evolution finally brought about the
form of life we know today. One of key arguments
against a model of evolution based on the accidental
changes of isolated genes is the simple fact that
gene mutation is a relatively rare event and hence,
according to this model, evolution would be very
slow. Many evolutionists argue that life on the
Earth would still be at the bacteria and seaweed stage, if genetic changes were based only on accidental
changes of isolated genes. Considering the
fact that most mutations are sources of negative
selective pressure, the minor percentage of accidental
mutations of genes that might cause positive
selective pressure, theoretically, could not
result in the evolution of living beings and the
diversity of species that we know today. Certainly,
this opinion does not completely exclude participation
of accidental isolated gene changes in the evolutionary
processes, but the influence of these
events on the evolution of life probably is minimal
and marginal [3,4,6].

With the exception of the mutations of isolated
genes, several different mechanisms can lead to
genome changes. These mechanisms are recombination,
transposition, translocations, inversions,
deletions, duplications, transduction and other
unpredictable, chaotic and yet unremarkable genetic
events which, in contrast to mutations, lead
to great changes of genome. Significant genetic
changes can probably result in ‘‘great evolutionary
displacement’’ and acceleration of evolutionary
processes. Incidentally, this hypothesis might represent
an acceptable explanation for the many
‘‘missing links’’ in palaeontology and the state of
our knowledge regarding the origin of life and species.
Put quite simply, what we call the ‘‘missing
links’’ probably never existed, due to ‘‘rapid’’
and large-scale changes which, for as yet unknown
reasons, have implicated, from time to time, every
living creature in the last billion years. Consequently,
we can conclude that the evolution of living
beings probably has not been based on gradual
and ‘‘fine’’ passing forms. In this story, viruses
could be an important factor in the theory of ‘‘rapid
and big evolutionary steps’’ based on great
changes of genome. Several mechanisms might be
included in this evolutionary scheme: (i) horizontal
transmission of genes between individuals of identical
or even different species; (ii) vertical transmission
of genes and bi-directional vertical
transmission between mother and offspring in
viviparous species; (iii) genome destabilization
and induction of new changes of genome; (iv)
increasing genome instability. Finally, the advantages
of the rapid evolution of living beings and a
possible link of this phenomenon with viruses could
be an acceptable explanation for the ‘‘symbiotic’’
connection of the genomic ability to emit DNA/RNA
sequences and/or de novo created viruses. This
phenomenon could lead to evolutionary conservation
of genome instability as a universal genome
characteristic [6,7].

Recombination is a far more powerful way for
DNA to change. This model of genome remodelling
takes whole blocks of genes and moves them to different
locations. These new locations could be
elsewhere in the same genome or in the genome
of a different host. One of recombination mechanisms
is transduction by viruses that works in both
prokaryotic and eukaryotic organisms. The discovery
that large blocks of genetic instructions can
be swapped and transferred among living beings
is a clue that the insertion of new genes could be
the mechanism that assists evolution. If viruses
can transfer eukaryotic genes across species
boundaries, and can install their own genes into
their hosts, the case for the new mechanism is even
stronger. Viruses do just that [1,3,4,6,7].

Viruses as natural biological weapon

From the standpoint of medical science, instability
is a highly undesirable feature of a genome as
it is very often a source of malignant alteration
of cells, spontaneous abortion, autoimmunity,
genetic diseases, emerging and even the reemerging
of new viruses. In contrast to this,
speaking in a Darwinian sense, the evolutionary
advantages of genome instability are probably
more important than potential and real negative
consequences of this phenomenon. In addition,
emitted DNA/RNA sequences and/or de novo created
viruses can operate as natural biological
weapons against predator and/or concurrent species.
This possibility could also be the source of
positive selective pressure supporting evolutionary
conservation of features such as genome
instability and its ability to emit its own sequences
[8–11].

Viruses apparently can, and obviously do, make
big jumps in hosts every now and then. It seems almost
certain, for example, that arthropods are the
original source for a number of virus families
infecting insects and mammals – such as the Flaviviridae
– and probably also of viruses infecting insects
and other animals and plants – such as the
Rhabdoviridae and Reoviridae. For example, picornaviruses
of mammals are very similar structurally
and genetically to a large number of small RNA
viruses of insects and to at least two plant viruses,
and – as the insect viruses are more diverse than
the mammalian viruses – probably had their origin
in some insect that adapted to feed on mammals
(or plants) at some distant point in evolutionary
time. The majority of existing viruses relevant to
humankind are zoonozis. In spite of the fact that
animals are the source of many viruses pathogenic
to humans, the most important factor in the dissemination of viruses is the fact that humans
live in a manner which increases the possibility of
transmission of new viruses from their endogen
hosts (animals) to humans. Rodents and arthropods
are also included in transmission of viruses from
one species to another, especially in an urban
milieu where their vector role is multi-amplified.
Other animals, especially primates, represent
important sources of viruses potentially pathogenic
for humans. In this context, we can mention a few
emerging or even re-emerging, new extremely
virulent and dangerous viruses which cause diseases
such as Ebola, Marburg and Congo-Crimean
haemorrhagic fever, Hantavirus lung syndrome,
Korean haemorrhagic disease, SARS-Co virus, and
of course, HIV1 and HIV2 [1,3,4,7].

HIV is important problem for humankind and
also a good example that can support our hypothesis
on viruses as natural biological weapons. It is
now generally accepted that HIV is a descendant
of simian immunodeficiency virus (SIV). Certain
simian immunodeficiency viruses bear a very close
resemblance to HIV-1 and HIV-2. For example,
HIV-2 corresponds to a simian immunodeficiency
virus found in the sooty mangabey monkey
(SIVsm), widely known as the green monkey,
which is indigenous to western Africa. The more
virulent strain of HIV, namely HIV-1, was, until
very recently, more difficult to place. The closest
counterpart that had been identified was the simian
immunodeficiency virus that was known to infect
chimpanzees (SIVcpz), but there were
significant differences between it and HIV. In
addition, it was reported that frozen tissue taken
from a chimpanzee carried a simian virus (SIVcpz)
which was almost identical to HIV-1. The chimpanzee
came from a sub-group of chimpanzees
known as Pan troglodytes troglodytes, which were
once common in west-central Africa. It is claimed
by some researchers that this shows that these
chimpanzees were the source of HIV-1, and that
the virus at some point crossed species from chimpanzees
to humans. However, it was not necessarily
clear that chimpanzees were the original
reservoir for HIV-1 because chimpanzees are only
rarely infected with SIVcpz. Also, there is opinion
that wild chimps became infected simultaneously
with two simian immunodeficiency viruses (SIVs)
that had ‘‘viral sex’’ to form a third virus capable
of infecting humans and causing AIDS [12–15].
Sharp et al. [16] discovered that the chimp virus
was an amalgam of the SIV infecting red-capped
mangabeys and the virus found in greater spotnosed
monkeys. The authors believe that the
hybridisation took place inside chimps that had
become infected with both strains of SIV after
hunting and killing the two smaller species of
monkey [16].

The hypothesis that HIV evolved from SIV is
based on the many similarities between these
two viruses, especially at the genetic level. The
two viruses are genetically very similar and are
transmitted in the same way. However, HIV only
causes AIDS in humans and SIV only causes AIDS
in monkeys. The SIV virus, like HIV, is found in
blood. This can provide support for the belief
that HIV entered man via monkey’s blood. For
this, possible routes include drinking the blood
of monkeys, eating raw monkeys or perhaps direct
exposure of humans to monkey blood
[13,14,16]. Finally, the possibility of interspecies
sexual transmission cannot yet be excluded.

Conclusion

The opinion that viruses simply cause infectious
diseases is over-simplified and archaic. Their role
in nature and their influence on the evolution of
other living things is probably of greater and,
even, crucial importance. The ability of a genome
to emit de novo created viruses and the evident
evolutionary conservation of this property
strongly suggests that emitted DNA/RNA sequences
could be important in the evolution of
life. Practically, this means that viruses could
be important sources of positive selection pressure
on certain species, thus opening up the possibilities
of: (i) horizontal dissemination of genes;
(ii) rapid and large-scale evolutionary changes by
way of unstable genomes; (iii) a role as biological
weapons directed against concurrent and/or
predator species.

References

[1] Margulis L, Sagan D. Microcosmos: four billion years of
evolution from our microbial ancestors. University of
California Press; 1997.